Blackwell Science, LtdOxford, UKAJDAustralasian Journal of Dermatology0004-83802005 Blackwell Publishing Asia Pty LtdMay 2005462104105Case ReportPhoto-onycholysis due to sparfloxacinVK
Mahajan
and NL Sharma
Australasian Journal of Dermatology (2005) 46, 104–105
CASE REPORT
Photo-onycholysis due to sparfloxacin Vikram K Mahajan and Nand Lal Sharma Department of Dermatology, Venereology and Leprosy, Indira Gandhi Medical College, Shimla, India
SUMMARY This paper describes a case of sparfloxacin-induced photodermatitis associated with photo-onycholysis in a 36-year-old man. He was being treated with sparfloxacin, streptomycin, ethambutol and pyrazinamide for pulmonary tuberculosis. He developed an exaggerated sunburn-like rash over the face and the dorsa of hands and feet, and painful onycholysis of fingerand toe-nails. Withdrawal of sparfloxacin resulted in resolution of the skin rash and nail tenderness. Key words: fluoroquinolone, photodermatitis.
tosensitive rash in less than 2 weeks and a lichenoid tissue reaction after 2 weeks. The time from administration of sparfloxacin to the onset of cutaneous eruptions was 11– 281 days.3 Photo-onycholysis is sometimes associated with cutaneous photosensitivity and is mostly described with tetracyclines, psoralens and occasionally pefloxacin and ofloxacin.4 We present a case of photo-onycholysis associated with phototoxic dermatitis following sparfloxacin therapy. Although we have frequently seen cases of sparfloxacin-induced photodermatitis in our clinical practice, associated photo-onycholysis has been observed by us for the first time.
CASE REPORT
INTRODUCTION Cutaneous photosensitivity is a consistent, although uncommon, feature of fluoroquinolones. The phototoxic potential of fluoroquinolones increases depending on their biological half-life. The UVA wavelength has been implicated in their photosensitivity.1 Sparfloxacin, a fluoroquinolone, has broad-spectrum antibacterial activity against Gram-negative, Gram-positive and anaerobic organisms. It is also a second-line drug for the treatment of tuberculosis and leprosy. It is well known as a cause of photosensitivity, presumably phototoxicity, that appears to depend upon the dose and the amount of UV irradiation.2 Its higher phototoxic potential has been attributed to its longer biological half-life (16 hours), a significantly higher tissue concentration and high affinity to the skin in comparison with other fluoroquinolones.3 Sparfloxacin induced a photosensitive dermatitis in less than 2 weeks with a dose of 400 mg/day, while a dose of 200 mg/ day did not cause photosensitivity even when used for more than 2 weeks.4 However, other workers among patients consuming sparfloxacin 200 mg/day have observed a pho-
Correspondence: Dr NL Sharma, Department of Dermatology, Venereology and Leprosy, Indira Gandhi Medical College, Shimla 171001 (HP), India. Email:
[email protected] Vikram K Mahajan, MD. Nand Lal Sharma, MD. Submitted 14 April 2004; accepted 4 November 2004.
A 36-year-old dark-skinned (type-V skin) Indian man presented with a facial rash. He had been on treatment with oral sparfloxacin 400 mg/day, along with ethambutol, pyrazinamide and intramuscular streptomycin in standard doses for multi-drug-resistant pulmonary tuberculosis. History revealed that he had been treated for pulmonary tuberculosis on two separate occasions in the past, and had now again developed fever, chest pain, dyspnoea, productive cough and haemoptysis. His sputum examination showed Mycobacterium tuberculosis in direct smears as well as on culture. He also had corroborating findings on clinical examination, chest X-ray films and his erythrocyte sedimentation rate was 38 mm in the first hour (normal value is 5–10 mm in the first hour using the Westergren method). Within 4–5 days of this treatment he developed swelling of the face accompanied by redness and intense burning and itching. Over the next 10–12 days, while the facial rash increased, he also noticed similar changes over the dorsa of the hands and feet, and pain over all the nails. Cutaneous examination showed mild oedema and intense, diffuse erythema over the forehead, malar area, chin, and the dorsa of the hands and feet. In places vesiculation, darkening and desquamation of the skin was suggestive of an acute sunburn-like reaction. All the finger-and toe-nails were tender, and showed irregular whitening and separation of the distal half of the nail plate from the nail bed with a proximal inflammatory band (Fig. 1). The hair and mucous membranes were normal. Other systemic examination did not reveal any abnormality.
Photo-onycholysis due to sparfloxacin
Figure 1 Photo-onycholysis right-hand finger nails.
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With the diagnosis of sparfloxacin-induced photo-onycholysis and phototoxic dermatitis, the drug was substituted with rifampicin. On a subsequent review, 4 weeks after stopping sparfloxacin, facial erythema and oedema had subsided with desquamation and hyperpigmentation, while onycholysis without pain or the proximal inflammatory band was persisting. Further follow up was unavailable.
DISCUSSION The events leading to disruption of the subungual cementing substance or damage to the surrounding supporting structures predisposes for onycholysis. Photo-onycholysis through phototoxic mechanisms is a well-known complication of a number of drugs, including flouroquinolones.5 Onycholysis induced purely by solar irradiation is not seen, despite the fact that the nail and the nail bed do not contain melanin, which might otherwise offer some photoprotection. Evidently, the nail plate, due to its reflective, refractive and absorptive properties, does offer some protection to the nail bed from solar damage unless it is predisposed to photodamage, as after some medication. The photodamage to the biological substrate is then initiated by absorption of the appropriate wavelength (action spectrum) by the photosensitizer. Thus painful onycholysis and a sunburn-like skin reaction after sparfloxacin therapy in our patient appears to be induced by sparfloxacin phototoxicity. Streptomycin, ethambutol and pyrazinamide are not known photosensitizers. The action spectrum for photoonycholysis lies in the UVA region, as UVB does not reach the nail bed.6 As UVA has also been implicated in fluoroquinolone photosensitivity reactions, it can reasonably be
postulated that sparfloxacin-induced photo-onycholysis is due to UVA irradiation. The interaction of non-ionizing radiation, the photosensitizing chemicals, and the affected biological structures occur as a result of photodynamic (oxygen-dependent, e.g. porphyrin phototoxicity) or non-photodynamic (oxygenindependent, e.g. psoralen phototoxicity) reactions. Photoinduced cellular damage results from phototoxicity to either cellular DNA/RNA, as with psoralens, or mitochondria, as with tetracycline.7 However, the exact pathomechanism of phototoxic onycholysis remains a matter of conjecture.
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